【摘要】 目的探讨p38抑制剂在RSV感染后激素不敏感中的作用。方法 RSV滴鼻建立RSV感染动物模型,分别腹腔注射地塞米松、地塞米松+MAPK(p38、ERK、JNK)抑制剂处理,处理7 d后肺泡灌洗液细胞计数及分类计数,ELISA检测肺泡灌洗液中IFN-γ、IL-6水平,肺功能仪检测气道高反应。结果地塞米松不能抑制RSV感染引起的气道炎症细胞浸润及气道高反应,地塞米松增加肺泡灌洗液中性粒细胞数量及IL-6水平而不能抑制IFN-γ的水平。予以MAPK抑制剂处理后均不能改变地塞米松对RSV感染后气道炎症及AHR的作用,但p38抑制剂能降低地塞米松对中性粒细胞的募集及IL-6的增高。结论 p38抑制剂不能逆转RSV感染后激素的抗炎作用,但能影响激素对中性粒细胞的作用。更多还原

【Abstract】 This study was performed to investigate the role of p38 inhibitor in glucocorticoid treatment forRSV-induced airway inflammation and airway hyperreactivity(AHR). Mice were inoculated with RSV intranasally,then mice were injected intraperitoneally daily with either dexamethasone(DEX) or pretreated with MAPK inhibitorson day 0 to 6, consecutively. On day 7, AHR were detected, and bronchoalveolar lavage fluid(BALF) was collectedfor cytokine concentration measurement and inflammatory cell evaluation, and the BALF IFN-γ and IL-6 levelswere measured using mouse ELISA kits. Data showed that DEX did not suppress airway inflammation or AHR in theRSV-infected mice. Moreover, DEX increased neutrophil infiltration and IL-6 levels in the BALF of infected mice,but had no effect on IFN-γ levels. Pretreatment with MAPK inhibitors did not change the effect of DEX in treatingRSV-infected airway inflammation. But pretreatment with p38 inhibitor/decreased the neutrophil infiltration andIL-6 levels which caused by DEX treatment. These results showed that p38 inhibitor do not alter the sensitivity ofDEX in treating RSV-infected airway inflammation and AHR, but play a role in neutrophil recruitment.更多还原